tetano
Editor, Senior Moderator
Virusdisease
. 2024 Jun;35(2):329-337.
doi: 10.1007/s13337-024-00873-y. Epub 2024 May 27. p38-MAPK is prerequisite for the synthesis of SARS-CoV-2 protein
Priyasi Mittal[SUP] 1 2 [/SUP], Nitin Khandelwal[SUP] 1 [/SUP], Yogesh Chander[SUP] 1 [/SUP], Assim Verma[SUP] 1 [/SUP], Ram Kumar[SUP] 1 [/SUP], Chayanika Putatunda[SUP] 2 [/SUP], Sanjay Barua[SUP] 1 [/SUP], Baldev Raj Gulati[SUP] 1 [/SUP], Naveen Kumar[SUP] 1 [/SUP]
Affiliations
The inhibition of p38 mitogen-activated protein kinase (p38-MAPK) by small molecule chemical inhibitors was previously shown to impair severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) replication, however, mechanisms underlying antiviral activity remains unexplored. In this study, reduced growth of SARS-CoV-2 in p38-α knockout Vero cells, together with enhanced viral yield in cells transfected with construct expressing p38α, suggested that p38-MAPK is essential for the propagation of SARS-CoV-2. The SARS-CoV-2 was also shown to induce phosphorylation (activation) of p38, at time when transcription/translational activities are considered to be at the peak levels. Further, we demonstrated that p38 supports viral RNA/protein synthesis without affecting viral attachment, entry, and budding in the target cells. In conclusion, we provide mechanistic insights on the regulation of SARS-CoV-2 replication by p38 MAPK.
Keywords: Host-directed antivirals; Protein synthesis; SARS-CoV-2; SB203580; p38-MAPK.
. 2024 Jun;35(2):329-337.
doi: 10.1007/s13337-024-00873-y. Epub 2024 May 27. p38-MAPK is prerequisite for the synthesis of SARS-CoV-2 protein
Priyasi Mittal[SUP] 1 2 [/SUP], Nitin Khandelwal[SUP] 1 [/SUP], Yogesh Chander[SUP] 1 [/SUP], Assim Verma[SUP] 1 [/SUP], Ram Kumar[SUP] 1 [/SUP], Chayanika Putatunda[SUP] 2 [/SUP], Sanjay Barua[SUP] 1 [/SUP], Baldev Raj Gulati[SUP] 1 [/SUP], Naveen Kumar[SUP] 1 [/SUP]
Affiliations
- PMID: 39071879
- PMCID: PMC11269555 (available on 2025-06-01)
- DOI: 10.1007/s13337-024-00873-y
The inhibition of p38 mitogen-activated protein kinase (p38-MAPK) by small molecule chemical inhibitors was previously shown to impair severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) replication, however, mechanisms underlying antiviral activity remains unexplored. In this study, reduced growth of SARS-CoV-2 in p38-α knockout Vero cells, together with enhanced viral yield in cells transfected with construct expressing p38α, suggested that p38-MAPK is essential for the propagation of SARS-CoV-2. The SARS-CoV-2 was also shown to induce phosphorylation (activation) of p38, at time when transcription/translational activities are considered to be at the peak levels. Further, we demonstrated that p38 supports viral RNA/protein synthesis without affecting viral attachment, entry, and budding in the target cells. In conclusion, we provide mechanistic insights on the regulation of SARS-CoV-2 replication by p38 MAPK.
Keywords: Host-directed antivirals; Protein synthesis; SARS-CoV-2; SB203580; p38-MAPK.